title: Exploiting the stress response to radiation to sensitize poorly immunogenic tumors to anti-CTLA-4 treatment.
abstract: Radiotherapy sensitizes unresponsive tumors to the antineoplastic activity of antibodies that target the inhibitory receptor CTLA-4 on T cells. One molecular mechanism accounting for this therapeutic synergy is the induction of NKG2D ligands on irradiated tumor cells. The fact that NKG2D receptors must be engaged for the elicitation of CD8+T-cell antitumor responses has important clinical implications.
authors.affiliation: Department of Pathology; New York University School of Medicine; New York, NY USA ; Department of Radiation Oncology; New York University School of Medicine; New York, NY USA.
authors.forename: Sandra
authors.initials: S
authors.lastname: Demaria
authors.forename: Karsten A
authors.initials: KA
authors.lastname: Pilones
authors.forename: Silvia C
authors.initials: SC
authors.lastname: Formenti
authors.forename: Michael L
authors.initials: ML
authors.lastname: Dustin
keywords: CTLA-4; NKG2D; RAE-1; abscopal effect; ipilimumab; radiotherapy; synergy; tumor rejection